gms | German Medical Science

29. Wissenschaftlicher Kongress der Deutschen Hochdruckliga

Deutsche Hochdruckliga e. V. DHL ® - Deutsche Hypertonie Gesellschaft Deutsches Kompetenzzentrum Bluthochdruck

23. bis 25.11.2005, Berlin

Rat chromosome 19 of the SHR strain contains genetic factors that protect against salt-sensitive hypertension and cardiovascular hypertrophy in the Dahl SS rat

Das SHR Chromosom 19 enthält genetische Faktoren, die die Dahl SS Ratte gegen salz-sensitive Hypertonie und kardiovaskuläre Hypertrophie schützen

Meeting Abstract

  • N. Wendt - Charité - Universitätsmedizin Berlin, Campus Benjamin Franklin (Berlin, D)
  • M. Wehland - Charité - Universitätsmedizin Berlin, Campus Benjamin Franklin (Berlin, D)
  • J. Weiss - Charité - Universitätsmedizin Berlin, Campus Benjamin Franklin (Berlin, D)
  • A.K. Siegel - Charité - Universitätsmedizin Berlin, Campus Benjamin Franklin (Berlin, D)
  • A. Schulz - Charité - Universitätsmedizin Berlin, Campus Benjamin Franklin (Berlin, D)
  • R. Kreutz - Charité - Universitätsmedizin Berlin, Campus Benjamin Franklin (Berlin, D)

Hypertonie 2005. 29. Wissenschaftlicher Kongress der Deutschen Hochdruckliga. Berlin, 23.-25.11.2005. Düsseldorf, Köln: German Medical Science; 2006. Doc05hochP45

Die elektronische Version dieses Artikels ist vollständig und ist verfügbar unter: http://www.egms.de/de/meetings/hoch2005/05hoch045.shtml

Veröffentlicht: 8. August 2006

© 2006 Wendt et al.
Dieser Artikel ist ein Open Access-Artikel und steht unter den Creative Commons Lizenzbedingungen (http://creativecommons.org/licenses/by-nc-nd/3.0/deed.de). Er darf vervielfältigt, verbreitet und öffentlich zugänglich gemacht werden, vorausgesetzt dass Autor und Quelle genannt werden.


Gliederung

Text

Recently, we have identified a quantitative trait locus linked to cardiovascular hypertrophy in a salt-fed F2-population derived from salt-sensitive Dahl (SS) and spontaneously hypertensive (SHR) rats. This study sought to test the relevance of rat chromosome 19 (RNO19) for target organ damage in SS. We therefore generated a speed consomic stain in which RNO 19 from SHR was introgressed into the SS genetic background, thus creating the SS-19SHR strain.

Male animals (n=14-21) were studied either under a normal (0.2% NaCl) or a high salt diet (4% NaCl) beginning at 6 weeks of age for 8 weeks, respectively. All measurements were performed at the age of 14 weeks. Systolic blood pressure (SBP) measurements were performed on three consecutive days by tail-cuff method.

SBP in the salt-fed SS-19SHR was significantly lower compared to the SS rats (186 +/- 30 vs. 213 +/- 14 mmHg, p<0.0001). More importantly, the relative weight of the left ventricle in salt-fed SS-19SHR (2.50 +/- 0.28 mg/g) was similar to that of SHR (2.61 +/- 0.23 mg/g) and significantly reduced compared to SS (3.1 +/- 0.5 mg/g, p<0.00001). In addition, the relative weight of the aorta was also significantly lower in salt-fed SS-19SHR rats (1.41 +/- 0.24 mg/mm) compared to SS (1.65 +/- 0.2 mg/mm, p= 0.0046). These results show that there is at least one genetic locus on RNO19 that protects the SS rat against salt-induced progression of hypertension and cardiovascular hypertrophy